Object-Cooperated Ternary Tree Partitioning Decision Method for Versatile Video Coding.

In this paper, we propose an object-cooperated decision method for efficient ternary tree (TT) partitioning that reduces the encoding complexity of versatile video coding (VVC). In most previous studies, the VVC complexity was reduced using decision schemes based on the encoding context, which do not apply object detecion models. We assume that high-level objects are important for deciding whether complex TT partitioning is required because they can provide hints on the characteristics of a video. Herein, we apply an object detection model that discovers and extracts the high-level object features-the number and ratio of objects from frames in a video sequence. Using the extracted features, we propose machine learning (ML)-based classifiers for each TT-split direction to efficiently reduce the encoding complexity of VVC and decide whether the TT-split process can be skipped in the vertical or horizontal direction. The TT-split decision of classifiers is formulated as a binary classification problem. Experimental results show that the proposed method more effectively decreases the encoding complexity of VVC than a state-of-the-art model based on ML.

Stabilization of HDAC1 via TCL1-pAKT-CHFR axis is a key element for NANOG-mediated multi-resistance and stem-like phenotype in immune-edited tumor cells.

Cancer immunoediting enriches NANOG expression in tumor cells, resulting in multi-drug resistance and stem-like phenotypes. We previously demonstrated that these NANOG-associated phenotypes are promoted through HDAC1 transcriptional upregulation. In this study, we identified that NANOG also contributes to the stabilization of HDAC1 protein through the AKT signaling pathway. NANOG-AKT axis leads to phosphor-dependent inactivation of CHFR, an E3 ligase for HDAC1 protein, and thereby inhibiting the ubiquitin-mediated degradation of HDAC1. Furthermore, AKT inhibition disrupts HDAC1 WT-mediated phenotypes but had no effect on the phenotypes mediated by HDAC1 FM, a mutant that is unable to interact with CHFR. Critically, we applied a catalytic dead mutant, HDAC1-H141A, to uncover that HDAC1 confers immune-resistance, drug-resistance and stem-like phenotype in tumor cells through its catalytic activity. Collectively, our results establish a firm molecular link in immune-edited tumor cells among NANOG, AKT, CHFR, and HDAC1, identifying HDAC1 as a molecular target in controlling NANOGHIGH immune-refractory cancer.